Contracts for Model Execution Verification

International audienceOne of the main goals of model-driven engineering is the manipulation of models as exclusive software artifacts. Model execution is in particular a means to substitute models for code. We focus in this paper on verifying model executions. We use a contract-based approach to specify an execution semantics for a meta-model. We show that an execution semantics is a seamless extension of a rigorous meta-model specification and is composed of complementary levels, from static element definition to dynamic elements, execution specifications as well. We use model transformation contracts for controlling the dynamic consistent evolution of a model during its execution. As an illustration, we apply our approach to UML state machines using OCL as the contract expression language

Proved Metamodels as Backbone for Software Adaptation

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Dynamic Adaptive Software Components: the MOCAS Approach

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PauWare : un modèle de composants basé état

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Endowing software components with autonomic capabilities based on modeling language executability

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MOCAS: a state-Based components Model for Self-Adaptation

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Developmental cell death during Xenopus metamorphosis involves BID cleavage and caspase 2 and 8 activation.

International audienceElimination of tadpole organs during Xenopus metamorphosis is largely achieved through apoptosis, and recent evidence suggest involvement of the mitochondrial death route and bax-initiated caspase-3 and -9 deployment. However, events upstream of the activation of Bax are unknown. In other models, proteins of the BH3-only group such as BID are known to assure this function. We show that Xenopus bid transcript levels increase at metamorphosis in larval cells destined to disappear. This increase correlates with an abrupt rise in Caspase-2 and -8 mRNA levels and an enhanced activity of Caspase-2 and -8. In BIDGFP transgenic animal's tail regression is accelerated. The cleavage of BIDGFP fusion protein during natural or T(3)-induced metamorphosis was specifically inhibited by caspase-8 inhibitors. Our results show that tail regression at metamorphosis implicates an apoptotic pathway inducible by T(3) hormone in an organ autonomous manner and involving the cell death executioners BID and Caspases-2 and -8